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In Shewanella putrefaciens CN32, the carbon source sodium lactate negatively regulates biofilm formation via a three‑component system: LrbS (histidine kinase) senses lactate, activates LrbA (transcription factor), which upregulates LrbR (phosphodiesterase). LrbR reduces c‑di‑GMP levels, thereby inhibiting biofilm. This work elucidates a novel signaling pathway linking carbon source to biofilm control, with implications for other bacteria.
Fig. 1 Sodium lactate negatively regulates biofilm formation. (Liu C, et al., 2017)
References
In colorectal cancer, hypoxia-induced lactate accumulation led to histone lactylation, which promoted RUBCNL/Pacer transcription, facilitating autophagosome maturation via BECN1 interaction. Bevacizumab-resistant patients showed elevated histone lactylation. Inhibition of histone lactylation or autophagy combined with bevacizumab demonstrated remarkable efficacy in patient-derived preclinical models. This study links metabolic reprogramming to epigenetic regulation and provides a new strategy to improve bevacizumab efficacy in CRC.
Fig. 2 Colorectal cancer (CRC) resistance to bevacizumab treatment exhibited increased lactylation levels which was associated with poor survival in CRC patients. (Li W, et al., 2024)
References
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